Summary Research Q8 - Renal Disorders (AKI), including lectures and one GW.
*2017/2018 summary: might not fully cover all the subjects from the current year anymore.
This summary no longer corresponds to the current substance for this module.
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Renske de Veer (rdeveer)
Summary Renal disorders
HC 1: Clinical forms and aspects of AKI
Acute kidney injury (AKI)
- Abrupt decrease of kidney function over a period of 7 days or less
o Occurs in 7-18% of the patients in the hospital. Occurs in 50% of patients admitted to
the ICU (50% of these patients die). → worldwide 2 million people die as a result of
AKI every year.
- AKI causes a build-up of waste products in your blood and makes it hard for your kidneys to
keep the right balance of fluid in your body. AKI can also affect other organs such as the
brain, heart, and lungs
- Based on rise in serum creatinine (renal biomarker) or an episode of oliguria (urine
production of 400 ml or less)
o Higher stage of AKI when the urine output is lower
- Caused by:
o Renal hypoperfusion → ischemia
▪ Gross blood loss
▪ Severe fluid loss from the GI tract
▪ Microcirculatory dysfunction
o Systemic and renal inflammation
o Nephrotoxic agents
▪ Iodinated contrast mediated (used when making CT scan of aorta)
▪ Drugs
- Complications of AKI
o Fluid overload (kidneys function to remove waste products/fluids)
o Bleeding due to impaired coagulation (decreased function of platelets)
o Development of chronic kidney disease
▪ Cardiovascular complications
▪ Mortality
- Treatment of AKI
o Optimization of hemodynamic status
▪ Avoid hypoperfusion (maintain blood pressure) and overhydration
o Avoid nephrotoxic (drugs etc) insults
o Renal replacement therapy
o Currently no drugs to treat AKI
➔ Kidney: filtration of blood in the glomarus. (118L of urine per day) → concentrating system
that is responsible for production of 2L urine, the rest is reabsorbed (e.g. water and other
molecules that you do not want to lose, such as sodium and amino acids) → oxygen (& ATP)
is required.
,Renske de Veer (rdeveer)
➔ Sodium reabsorption: Sodium passes along an electrochemical gradient (passive transport)
from the lumen into the tubular cell, together with water and chloride which also diffuse
passively. Water is reabsorbed to the same degree, resulting in the concentration in the end
of the proximal tubule being the same as in the beginning → the reabsorption in the
proximal tubule is isosmotic.
Kidney is the highest oxygen consumer in the body. → hypoperfusion of tissue → kidney becomes
damaged.
➔ Formation of ROS after reperfusion. Reactive oxygen species formation in the kidney likely
plays a significant role in the genesis acute injury. Evidence has implicated ROS activity as
being important in AKI in models of ischemia/reperfusion, cisplatin, mercury, gentamicin,
endotoxin and glycerol . (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919808/)
➔ Degradation of ATP to ADP to hypoxanthine. Reperfusion of oxygen causes the formation of
radical oxygen species → tissue damage.
Renal replacement therapy
, Renske de Veer (rdeveer)
Renal replacement therapy (RRT) is therapy that replaces the normal blood-filtering function of the
kidneys. It is used when the kidneys are not working well and includes acute kidney injury and
chronic kidney disease. Renal replacement therapy includes dialysis (hemodialysis or peritoneal
dialysis), hemofiltration, and hemodiafiltration, which are various ways of filtration of blood with or
without machines. Renal replacement therapy also includes kidney transplantation, which is the
ultimate form of replacement in that the old kidney is replaced by a donor kidney.
Biomarkers (current biomarkers; creatinine (present late in disease, rises when renal function
decreases)
- Allow early identification of patients at high risk for AKI
- Monitor treatment strategies to prevent mitigate AKI → molecules involved in
pathophysiology
- To discriminate between different causes of AKI
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